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Fig. 8. Ectopic expression of Doc together with pnr and
tin promotes cardioblast specification. (A-F) Cardioblasts of
representative stage 15-16 embryos labeled for mid mRNA and Mef2
protein. All images are projections of confocal scans merged as in
Fig. 5. (A) Wild-type embryo
showing single-cell bilateral rows of cardioblasts. (B) Ectopic expression of
Doc2 throughout the dorsal mesoderm using
tinD-GAL4/UAS-Doc2 produces extra cardioblasts (arrowheads).
(C) Combined expression of pnr+tin leads to a similar number
of supernumerary cardioblasts as with UAS-Doc2. (D) Combined
expression of Doc2+tin produces even more cardioblasts than
with UAS-Doc2 alone. (E) UAS-Doc2+UAS-pnr and (F)
UAS-Doc2+UAS-pnr+UAS-tin driven by
tinD-GAL4 produce the strongest increase in cardioblast number, with
almost twice as many cardioblasts as in wild type. (G) Lateral view of stage
14 wild-type embryo stained for mid mRNA and Mef2, showing a single
row of cardioblasts. (H) Embryo as in G, but with twi-GAL4-driven
expression of Doc2, pnr and tin, which shows a dramatic
expansion of myocardial mid expression (arrowhead). (I) Stage 16
wild-type embryo stained for the pericardial cell markers Zfh-1, Odd and Eve
as in Fig. 4A. (J)
tinD-GAL4/UAS-Doc2 embryo stained as in I, showing fewer
pericardial cells, especially of the Odd-PC type (yellow). Eve-PCs (pink) and
DA1 muscles (blue) are only mildly affected. A reduction of Odd+
cells is also seen in the lymph gland. (K) Combined expression of pnr
and tin in the dorsal mesoderm leaves the majority of the pericardial
cells intact, although some Eve-PCs and Odd-PCs are missing (bracket). (L)
Combined overexpression with
UAS-Doc2+UAS-pnr+UAS-tin leads to a severe
reduction of all types of pericardial cells, although Eve-PCs (pink) are
retained more frequently.
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